Respiratory System PDF

Respiratory System 1  The Respiratory System The upper respiratory tract consists of the nose, mouth, sinuses, pharynx, and larynx. The lower respiratory tract consists of the trachea, bronchi and bronchioles, and lungs....

Respiratory System 1  The Respiratory System The upper respiratory tract consists of the nose, mouth, sinuses, pharynx, and larynx. The lower respiratory tract consists of the trachea, bronchi and bronchioles, and lungs. 2  Upper respiratory tract infection (URTI) Are the illnesses caused by an acute infection which involves the nose, sinuses, pharynx or larynx. Commonly caused by viruses & some times bacteria. URTI includes: i. Rhinosinusitis (common cold) ii. Sinusitis iii. Pharyngitis / tonsilitis iv. Laryngitis 3  Symptoms of URTI Nasal congestion Cough Running nose Sore throat Fever Sneezing Onset of the symptoms usually begins after 1-3 days after exposure to a microbial pathogen. The duration of the symptoms is typically 7 to 10 days but may persist longer. 4  Acute Bronchitis Superficial inflammation of the bronchi. Causes: viruses, bacterial, irritant inhalation, and allergic reactions. Considered as acute illness. In non-smokers, bronchitis is usually caused by a virus or bacteria that has first infected the nasal passages and upper airways, and then progressed into the chest. 5  Bronchitis Pathophysiology Hypertrophy and hyperplasia of mucus secreting glands. loss of cilia  mucus accumulation + reduce clearance of particles and microorganisms  increases risk of infection. 6 Bronchitis 7  Chronic Obstructive Pulmonary Disease (COPD) Chronic disorders characterized by irreversible airway obstruction. Severe hypoxia and hypercapnia can lead to respiratory failure. Causes: smoking, pollution, chemical irritants, and genetic mutation. Two main conditions: Chronic bronchitis and Emphysema. 8  Chronic Bronchitis Characterized by inflammation of the bronchi, productive cough, and excessive mucus production. A clinical diagnosis of chronic bronchitis requires the history of a chronic productive cough for at least 3 months in at least 2 consecutive years. 9  Emphysema Destruction of the alveolar walls, and loss of lung elasticity leads to large, permanently inflated alveoli. Causes: Inherited conditions (deficiency of α1-antitrypsin), and smoking. 10 Emphysema 11  Bronchial Asthma Chronic disorder that results in intermittent, reversible airway obstruction. Characterized by: 1. Airways constriction. 2. Airway inflammation. 3. Airways lined with excessive amounts of mucus. 12  Triggers of Bronchial Asthma An allergen Respiratory tract infection Environmental tobacco smoke Exercise or exertion Emotional stress Drugs (aspirin, beta blockers, and penicillin) Air pollution, and Cold environment. 13  Bronchial Asthma Symptoms: Wheezing Shortness of breath Chest tightness Coughing The symptoms of asthma can range from mild to life threatening. Life-threatening, prolonged asthma attack that does not respond to usual treatment called Status Asthmaticus. 14 Bronchial Asthma 15  Bronchiectasis Localized, irreversible dilatation of part of the bronchial tree. The involved bronchi are dilated, inflamed, and easily collapsible  resulting in airflow obstruction + impaired clearance of secretions. Causes include: 1. Congenital damage to the bronchiolar muscle and CT. 2. Damage 2ry to necrosis associated with recurrent infections. 16  Types of Bronchiectasis I. Fusiform (cylindrical) most common type mildly inflamed bronchi that fail to taper distally II. Varicose bronchial walls appear beaded, because areas of dilatation are mixed with areas of constriction III. Saccular (cystic) severe and irreversible ballooning of the bronchi peripherally, with or without air-fluid levels 17 Bronchiectasis 18  Atelectasis Defined as a state in which the lung, in whole or in part, is collapsed or without air. Causes: 1. Blockage of a bronchiole or bronchus can be: i. Within the airway (foreign body, mucus plug). ii. Compressing from the outside (tumor, lymph node, tubercle). 2. Post-surgical atelectasis. 3. Smokers & elderly subjects are at high risk. 19 Atelectasis 20  Pneumonia An infection of the small air sacs of the lungs (alveoli) and the tissues around them. Symptoms include: Cough with thick and colored sputum Fever, chills Chest pain Tiredness, weakness, muscle aches Noisy or painful breathing Shortness of breathing 21 Pneumonia 22  Classification of Pneumonia 1. According to the setting of the disease: Community-acquired pneumonia Hospital-acquired pneumonia 2. According to the causative agent: Bacterial pneumonia Viral pneumonia Mycoplasma pneumonia 3. According to distribution of the infection: Lobar pneumonia Bronchopneumonia 23  Aspiration Pneumonia Causes: After head injury General anesthesia When a pt takes drugs or alcohol In such cases, the gag reflex doesn't work as well as it should, so bacteria can enter the airways Bacteria that cause aspiration pneumonia are called anaerobic bacteria 24  Tuberculosis (TB) TB is a common and deadly infectious disease Caused by acid fast bacilli (mycobacterium tuberculosis) Acquired by air-borne infection resulting in granulomatous lesion TB most commonly attacks: lungs (as pulmonary TB) CNS Lymphatic system Circulatory system Genitourinary system Bones, Joints, and skin 25 Tuberculosis 26  Types of Pulmonary TB 1. Primary TB: lesion is called Ghon focus occurs in the lung. 2. Miliary TB: wide dissemination into the human body with presence of tiny size lesions (1-5 mm). It is a complication of 1-3% of all TB cases. 27  Pulmonary Embolism Obstruction of pulmonary artery or branch by blood clot. Obstructed area has diminished or absent blood flow. Risk factors include: Deep vein thrombosis. Certain disease states: heart disease (HF), trauma (fracture of hip), postoperative (orthopedic surgery), postpartum. Other conditions: Advance age (>50 years), pregnancy, obesity. Clinical Manifestations: Dyspnea, tachypnea, chest pain, tachycardia, hemoptysis. 28  Pleuritis Also called pleurisy. Acute inflammation of the pleura. Characterized by severe pain that worsen by deep breathing, coughing, or sneezing. It is not a disease by itself but complication of other diseases like viral respiratory infection or pneumonia. 29  Pleural Effusion Is an excess accumulation of fluid in the pleural space around the lungs. There are two major types of pleural effusion: 1. Transudative effusions, where the excess pleural fluid is low in protein. 2. Exudative effusions, where the excess pleural fluid is high in protein. 30 Pleural Effusion 31  Other Respiratory Diseases Pyothorax : Purulent fluid in the pleural cavity due to chest infection Hydrothorax: serous fluid accumulating in the pleural cavity due to liver cirrhosis Hemothorax: Hemorrhagic fluid in the pleural cavity due to malignant tumors 32  Pneumothorax Potential medical emergency caused by accumulation of air or gas in the pleural cavity, which leads lung collapse. Types include: 1. Spontaneous: occurs with or without lung disease like in asthma, TB, and tumors. 2. Tension: air in the pleural cavity due to a tear in the lung tissue  air accumulates in the pleural space with each breath  increase in intrathoracic pressure  shifts of the mediastinum away from the affected lung 33 Pneumothorax & Hemothorax 34 Pneumothorax 35  Pulmonary Edema Abnormal accumulation of fluid in the lung tissue, the alveolar space, or both. Rapid shift of fluid from the plasma to pulmonary interstitial tissue and alveoli. Leads to impaired gas exchange. Clinical manifestations: Dyspnea, air hunger, central cyanosis, Anxiety, agitation, blood-tinged sputum. 36  Acute Respiratory Distress Syndrome (ARDS) Severe inflammatory process causing diffuse alveolar damage that result in A sudden and progressive Pulmonary edema Results from rapid fluid accumulation in the alveoli due to a systemic or pulmonary event that is not cardiac in origin. Consequences includes Alveoli filled in fluids, Severe dyspnea, Hypoxemia, and Reduced lung compliance. 37  Respiratory Failure A sudden and life-threatening deterioration of the gas exchange function of the lung, and leads to failure of lung to provide adequate oxygenation for the blood. A result of inadequate gas-exchanging function. Caused by many conditions: COPD, asthma, ARDS, neuromuscular dysfunction disorders, brain hemorrhage, head trauma, chest trauma. Respiratory failure can be Acute or chronic Resp. Failure can be classified as Hypoxemic or Hypercapnic. 38 The End 39 Cardiovascular System 40  Disorders of the pericardium The pericardium isolates the heart from other thoracic structures, maintains its position in the thorax, and prevents it from overfilling. The two layers of the pericardium are separated by a thin layer of serous fluid, which prevents frictional forces from developing between the visceral and parietal layers of the pericardium. Pericardium disorders include pericarditis, pericardial effusion, and cardiac tamponade. 41  Pericarditis Pericarditis represents an inflammatory process of the pericardium. It can result from a number of diverse causes such as: infections, uremia, rheumatic fever, connective tissue diseases, and myocardial infarction. Classified as acute, chronic, and constrictive. 42  Pericardial Effusion Normally, there is about 30 to 50 mL of thin, clear, straw-coloured fluid in the pericardial sac. Pericardial effusion refers to the accumulation of fluid in the pericardial cavity. Small pericardial effusions may produce no symptoms or abnormal clinical findings. However, a sudden accumulation of even 200 mL may increase intracardiac pressure, compress the heart, and interfere with venous return to the heart. 43  Cardiac Tamponade Cardiac tamponade is a life-threatening condition represents an increase in intrapericardial pressure caused by an accumulation of fluid or blood in the pericardial sac. It can occur as the result of conditions such as trauma, cardiac surgery, cancer, uraemia, myocardial infarction. The seriousness of cardiac tamponade results from impairment in diastolic filling and reduction in stroke volume and cardiac output. 44 Clinical manifestation of Cardiac Tamponade Rapid accumulation of fluid results in an elevation of central venous pressure, jugular venous distention, a decline in venous return to the heart, a decrease in cardiac output despite an increase in heart rate, a fall in systolic blood pressure, pulsus paradoxus, and signs of circulatory shock. Pulsus paradoxus refers to decrease in systolic blood pressure (>10 mm Hg) during inspiration, is a clinical indicator of cardiac tamponade. 45 Coronary Heart Disease The term coronary heart disease (CHD) describes heart disease caused by impaired coronary blood flow. In most cases, CHD is caused by atherosclerosis. Diseases of the coronary arteries can cause angina, myocardial infarction or heart attack, cardiac dysrhythmias, conduction defects, heart failure, and sudden death. 46 Pathogenesis of Coronary Heart Disease 47  Angina Pectoris Angina pectoris is characterized by recurring episodes of chest pain or pressure sensation associated with myocardial ischemia. The hallmark symptom of angina is chest pain. Classified to: 1. Stable Angina. 2. Unstable Angina. 3. Vasospastic Angina. 48 49 50  Myocarditis The term myocarditis is used to describe an inflammation of the heart muscle and conduction system without evidence of myocardial infarction. The manifestations of myocarditis vary from an absence of symptoms to profound heart failure or sudden death. Acute symptomatic myocarditis typically manifests as a flulike syndrome with malaise, low-grade fever, and tachycardia. There commonly is a history of an upper respiratory tract or gastrointestinal tract infection, followed by a latent period of several days. 51  Cardiomyopathy Dilated cardiomyopathies: are characterized by progressive cardiac hypertrophy and dilation and impaired pumping ability of one or both ventricles. Although all four chambers of the heart are affected, the ventricles are more dilated than the atria. Dilated cardiomyopathy may result from a number of different myocardial insults, including infectious myocarditis, alcohol and other toxic agents, metabolic influences, neuromuscular diseases, and immunologic disorders. Genetic influences have been documented in some cases. 52  Endocarditis Infective endocarditis is a relatively uncommon, life-threatening infection of the endocardial surface of the heart, including the heart valves. Because bacteria are the most common infecting organisms, the condition may be referred to as bacterial endocarditis. Two factors contribute to the development of infective endocarditis: a damaged endocardial surface and a portal of entry by which the organism gains access to the circulatory system. The pathophysiology of infective endocarditis involves the formation of intracardiac vegetative lesions that have local and distant systemic effects. The vegetative lesion that is characteristic of infective endocarditis consists of a collection of infectious organisms and cellular debris. 53  Rheumatic Heart Disease Rheumatic fever is an acute, immune-mediated, multisystem inflammatory disease that follows a group A (-hemolytic) streptococcal (GAS) throat infection. Rheumatic fever can manifest as an acute, recurrent, or chronic disorder, Based on the duration of symptoms. The acute stage of rheumatic fever includes a history of an initiating streptococcal infection and subsequent involvement of the connective tissue of the heart, blood vessels, joints, and subcutaneous tissues. Common to all is a lesion called the Aschoff body, which is a localized area of tissue necrosis surrounded by immune cells. 54  Valvular Heart Disease Stenosis represents the incomplete opening, Which leads to: 1. Distention and increased work demands of the heart chamber that empties blood. 2. Impaired filling of the chamber that receives blood. Regurgitation is characterized by incomplete closure, Which leads to distention and places increased work demands on the chamber ejecting blood. 55  Heart Failure Condition result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with blood or pump a sufficient amount of blood through the body. Classified according to side: 1. Right sided heart failure 2. Left sided heart failure. 56  Classification of Heart Failure 1. Rt–sided (congestive) cardiac failure The Rt ventricle falls to empty when the pressure developed due to contraction cannot force blood out to the lungs. Decreased cardiac output and systematic congestion. Edema and weight gain. 2. Lt–sided (left ventricular) failure When the pressure developing in the left ventricle is less than the pressure in the aorta, and blood is not forced out fully. Decreased cardiac output and pulmonary congestion. Pulmonary Edema and dyspnea. 57  Cardiogenic Shock Shock: Inadequate blood flow to tissues and cells of the body. Cardiogenic shock: Left ventricle cannot maintain adequate cardiac output. Causes: Heart failure myocardial infarction, arrhythmias. Complications: Acute respiratory distress syndrome, renal failure, cerebral hypoxia, and death. 58 Alteration in Blood Flow 59  Atherosclerosis Atherosclerosis is a type of arteriosclerosis or hardening of the arteries. The term atherosclerosis denotes the formation of fibrofatty lesions in the intimal lining of the large and medium-size arteries such as the aorta and its branches, the coronary arteries, and the large vessels that supply the brain. 60  Risk Factors For Atherosclerosis Non modifiable: Age ( >45y for men, >55y for women), Gender ( men > women), Hereditary (Family History). Modifiable: High LDL, Low HDL, Hypertension, Smoking, Diabetes, Physical inactivity, Obesity, Stress. 61 Atherosclerosis 62 Atherosclerosis 63  Pathology and Pathogenesis The lesions associated with atherosclerosis are of three types: 1. The fatty streak 2. The fibrous atheromatous plaque 3. The complicated lesion. The latter two are responsible for the clinically significant manifestations of the disease. 64 Cont.… Fatty streaks are thin, flat yellow intimal discolorations that progressively enlarge by becoming thicker and slightly elevated as they grow in length. The fibrous atheromatous plaque is the basic lesion of clinical atherosclerosis. It is characterized by the accumulation of intracellular and extracellular lipids, proliferation of vascular smooth muscle cells, and formation of scar tissue. The more advanced complicated lesions are characterized by haemorrhage, ulceration, and scar tissue deposits. Thrombosis is the most important complication of atherosclerosis. 65  Varicose Veins Defined as abnormally dilated and tortuous superficial veins of the leg. This is in response to a pathological increase in the vein’s intraluminal pressure within the deep veins. Are more common in women than in men. 66 Varicose Veins 67 Varicose Veins 68 Varicose Veins 69 Varicose Veins 70  Varicose Veins RiskFactors: Hereditary Multiple pregnancies Obesity Aging Prolonged standing Abdominal straining 71 Varicose Veins 72  Deep Vein Thrombosis Blood clot in a deep vein of the upper (arm or neck) or lower (leg or pelvic) extremities. It differs from superficial thrombophlebitis which is an inflammation of the vein wall and formation of thrombus. 73 Deep Vein Thrombosis 74 75  Deep Vein Thrombosis Virchow’s triad outlines the three factors important in producing DVT: 1. Venous Stasis 2. Hypercoagulable Blood 3. Endothelial Injury 76  Virchow’s triad Three factors (Virchow’s triad): 1. Endothelial Injury: Trauma, surgery. 2. Venous stasis: Bed rest / immobilization, obesity, age (>65 years). 3. Hypercoagulable blood: Cancer, autoimmune disorders , platelet disorders. 77  One of the most common complication developed after Deep vein thrombosis is Pulmonary Embolism. 78  Pressure Ulcers Pressure ulcers are ischemic lesions of the skin and underlying structures caused by external pressure that impairs the flow of blood and lymph. Pressure ulcers often are referred to as decubitus ulcers or bedsores. Pressure ulcers are divided into four stages, according to the depth of tissue involved. Pressure ulcers are most likely to develop over a bony prominence, but they may occur on any part of the body that is subjected to external pressure, friction, or shearing forces. 79  Mechanisms of Development Two factors contribute to the development of pressure ulcers: 1. External pressure that compresses blood vessels. 2. Friction and shearing forces that tear and injure blood vessels. External pressure that exceeds capillary pressure interrupts blood flow in the capillary beds. When the pressure between a bony prominence and a support surface exceeds the normal capillary filling pressure, capillary flow essentially is obstructed. If this pressure is applied constantly for 2 hours, oxygen deprivation coupled with an accumulation of metabolic end products leads to irreversible tissue damage. 80  Prevention Methods for preventing pressure ulcers include: Frequent position change. Meticulous skin care. Frequent and careful observation. Adequate hydration of the stratum corneum. Prevention of dehydration. Maintenance of adequate nutrition. 81  Compartment Syndrome Compartment syndrome is a condition of increased pressure in a muscle compartment that compromises blood flow and potentially leads to death of nerve and muscle tissue. The "5 P's" are oftentimes associated with compartment syndrome: 1. Pain 2. Pallor (pale skin) 3. Paresthesia (numbness feeling) 4. Pulselessness (faint pulse) 5. Paralysis (weakness with movements) 82 Alteration in Blood Pressure 83  BLOOD PRESSURE The arterial blood pressure reflects the rhythmic ejection of blood from the left ventricle into the aorta. It rises as the left ventricle contracts (Systole) and falls as it relaxes (Diastole). Is the amount of force on the walls of the arteries as the blood circulates around the body. In healthy adults, the highest pressure, called the systolic pressure, ideally is less than 120 mm Hg, and the lowest pressure, called the diastolic pressure, is less than 80 mm Hg. 84  Determinants Of Blood Pressure Blood pressure is determined by: 1. Cardiac output (stroke volume x heart rate) 2. Peripheral vascular resistance, which is affected by: a. Humoral control b. Sympathetic nervous system control c. Local Control 85 86  HYPERTENSION Prolonged elevation in blood pressure. Defined as a systolic blood pressure greater than 140 mmHg and a diastolic pressure of more than 90 mmHg. Risk factors: Advancing age, Ethnicity, Heredity (family history), Obesity, Physical inactive, Smoking, Excessive alcohol intake, High- sodium diet, Stress, Diabetes mellitus. Called Silent killer and symptoms include Headache, blurry vision, chest pain, frequent urination at night. 87  Essential Hypertension Also called primary hypertension, and Idiopathic hypertension. Characterized by a chronic elevation in blood pressure that occurs without evidence of other disease. Affect about 90-95% of cases. 88  Secondary hypertension Characterized by an elevation of blood pressure that results from some other disorder. Affect about 5-10% of cases. Causes: (1) Certain diseases and conditions such as: Renal Disease, Pheochromocytoma, Coartication of aorta, brain tumors, pregnancy, medications, thyroid dysfunction. 89  Secondary hypertension (2) Excessive levels of certain hormones Hyper secretion of aldosterone. Excess glucocorticoids in Cushing's syndrome. Elevated estrogen level in birth control pills. Hypersecretion of Antidiuretic hormone. 90  Systemic Hypertension Whether it is 1ry or 2ry hypertension, it could be: 1. Benign Slowly progressive increase in the pressure Occurs in 95% of cases 2. Malignant Rapidly progressive increase in the pressure Occurs in 5% of the cases 91  Malignant Hypertension A small number of persons with secondary hypertension develop an accelerated and potentially fatal form of the disease malignant hypertension. Malignant hypertension is characterized by sudden marked elevations in blood pressure, with diastolic values above 120 mm Hg 92  Orthostatic Hypotension Orthostatic or postural hypotension is an abnormal drop in blood pressure on assumption of the standing position. Blood pools in the lower part of the body; when the standing position is assumed, cardiac output falls, and blood flow to the brain is inadequate. Dizziness, syncope (i.e., fainting), or both may occur. Classification 1. Many authorities consider a drop in systolic pressure of 20 mm Hg or more or a drop in diastolic blood pressure of 10 mm Hg or more as diagnostic of the condition. 2. Some authorities regard the presence of orthostatic symptoms (e.g., dizziness, syncope) as being more relevant than the numeric decrease in blood pressure. 93  Orthostatic Hypotension Causes: A wide variety of conditions, acute and chronic, are associated with orthostatic hypotension. These include reduced blood volume, drug-induced hypotension (medications), aging, bed rest, and autonomic nervous system dysfunction. 94 The End 95 Renal System 96 Urinary System 97 Function 98 OBSTRUCTIVE DISORDERS Urinary obstruction can occur in persons of any age and can involve any level of the urinary tract from the urethra to the renal pelvis. 99  Causes of urinary tract obstruction The conditions that cause urinary tract obstruction includes Developmental defects Pregnancy Benign prostatic hyperplasia Tumors Kidney stones. 100 Cont.. The two most damaging effects of urinary obstruction are: 1. Stasis of urine, which predisposes to infection and stone formation. 2. Development of backpressure, which interferes with renal blood flow, destroys kidney tissue, and predisposes to hydronephrosis. 101 Cont.. The manifestations of urinary obstruction depend on the site of obstruction, the cause, and the rapidity with which the condition developed. Most commonly, the person has pain, signs and symptoms of urinary tract infection, and manifestations of renal dysfunction, such as an impaired ability to concentrate urine. Changes in urine output may be misleading because output may be normal or even high in cases of partial obstruction. 102  Renal Calculi The most common cause of upper urinary tract obstruction is urinary calculi. Although stones can form in any part of the urinary tract, most develop in the kidneys. Three major theories are used to explain stone formation: 1. The saturation theory. 2. The matrix theory. 3. The inhibitor deficiency theory. 103 1. The saturation theory The saturation theory states that the risk of stone formation is increased when the urine is supersaturated with stone components (e.g., calcium salts, uric acid, magnesium ammonium phosphate, cystine). Supersaturation depends on urinary pH, solute concentration, ionic strength, and complexation. Treatment is depending on stone type and includes adequate fluid intake and dietary modification. 104 2. The matrix theory The matrix theory proposes that organic materials, such as mucopolysaccharides, act as a nidus for stone formation. This theory is based on the observation that organic matrix materials can be found in all layers of kidney stones. 105 3. The inhibitor theory The inhibitor theory suggests that persons who have a deficiency of proteins that inhibit stone formation in their urine are at increased risk for stone formation. 106  Urinary Tract Infections Urinary tract infections (UTIs) are the second most common type of bacterial infections seen by health care providers. Most UTIs are caused by Escherichia coli. Bacteria can enter the kidneys either through the bloodstream or as an ascending infection from the lower urinary tract. Most infections are of the ascending type. Risk Factors: Female, urinary obstruction, neurogenic bladder, postmenopausal women; in men with diseases of the prostate, elderly persons, improper personal hygiene. Instrumentation and urinary catheterization are the most common predisposing factors for Hospital acquired UTIs. 107  Urinary Tract Infections Urinary tract infections involve both the upper and lower urinary tract structures. 1. Upper urinary tract infections tend to invade the tissues of the kidney pelvis, inciting an acute inflammatory response. 2. Lower urinary tract infections, the infecting pathogens tend to propagate in the urine and cause irritative voiding symptoms. Clinical Manifestations: may be asymptomatic, cloudy and foul- smelling urine, pain and burning on urination, frequency, urgency, nocturia, and Hematuria may present. 108  Glomerulonephritis Bilateral inflammatory disorder of the glomeruli that typically follows a streptococcal infection. Affects men more than women. Leading cause of renal failure. Inflammatory changes impair the kidneys’ ability to excrete waste and excess fluid. May be acute or chronic. 109  Renal Failure Renal failure is a condition in which the kidneys fail to remove metabolic end-products from the blood and regulate the fluid, electrolyte, and pH balance of the extracellular fluids. Classified as Acute or Chronic. The most common indicator of renal failure is azotemia, an accumulation of nitrogenous wastes (urea nitrogen, uric acid, and creatinine) in the blood. 110  Acute Renal Failure Acute renal failure represents a rapid, and sudden decline in renal function sufficient to increase blood levels of nitrogenous wastes and impair fluid and electrolyte balance. Generally reversable, if the causing factors can be corrected. Causes may be prerenal, intrarenal (intrinsic), postrenal. Divided into three phases: The onset phase, maintenance phase, recovery phase. 111  Causes of Acute Renal Failure 1. Prerenal: result from decreased blood flow to the kidney. Hypovolemia, Hemorrhage, Dehydration, Excessive loss of fluid due to burn injury, shock, Heart failure, sepsis, drugs. 2. Intrarenal (Intrinsic): result from condition that disrupt structures in the kidney. Acute tubular necrosis, Prolonged renal ischemia, Exposure to nephrotoxic drugs, Intratubular obstruction resulting from hemoglobinuria, Acute renal disease (acute glomerulonephritis, pyelonephritis). 3. Postrenal: result from disorders that interfere with urine elimination from the kidney. Bilateral ureteral obstruction, Bladder outlet obstruction. 112  Phases of Acute Renal Failure 1. The onset phase, which lasts hours or days, is the time from the onset of the precipitating event (e.g., ischemic phase of prerenal failure or toxin exposure) until tubular injury occurs. 2. The maintenance phase is characterized by a marked decrease in the GFR, causing sudden retention of endogenous metabolites such as urea, potassium, sulphate, and creatinine that normally are cleared by the kidneys. The urine output usually is lowest at this point. Fluid retention gives rise to edema, water intoxication, and pulmonary congestion. 3. The recovery phase is the period during which repair of renal tissue takes place. Its onset usually is heralded by a gradual increase in urine output and a fall in serum creatinine, indicating that the nephrons have recovered to the point where urine excretion is possible. 113  Chronic Renal Failure Chronic renal failure represents progressive and gradual destruction of kidney structure, producing a marked decrease in glomerular filtration rate (GFR). Generally Irreversible. Divided into four stages: diminished renal reserve, renal insufficiency, renal failure, end stage renal disease (ESRD). Treated by hemodialysis and peritoneal dialysis. 114  Causes of Chronic Renal Failure Diabetes mellitus. Hypertension. Chronic Glomerulonephritis. Chronic Pyelonephritis. Medication or toxic agents. Urinary tract obstruction. 115 Manifestations of Chronic Renal Failure 116 The End 117 Alterations in Fluids and Electrolytes 118  Fluids Approximately 60% of typical adult is fluid. Divided to: 1. Intracellular fluid (ICF): 2\3 of body fluid. 2. Extracellular fluid (ECF): 1\3 of body fluid. i. Intravascular: fluid in blood vessel: 3.5L is plasma. ii. Interstitial: fluid surround the cell: 10L (lymph). iii. Transcellular: 1L (as CSF, Intraocular, pericardial, pleural fluid, synovial fluid). 119  Electrolytes Active chemicals that carry positive (cations), negative (anions) electrical charges Major cations: sodium, potassium, calcium, magnesium, hydrogen ions. Major anions: chloride, bicarbonate, phosphate, sulfate. Electrolyte concentrations differ in fluid compartments (ICF &ECF). Sodium is the major electrolyte in the ECF. Potassium is the major electrolyte in the ICF. 120  Diffusion and Osmosis Diffusion is movement of solute (molecules and ions), and water from an area of higher concentration to an area of lower concentration. Osmosis is movement of fluid (water) across a semipermeable membrane from and area of lower solute concentration to an area of higher solute concentration. Osmolality is the concentration of solutes in body fluids. Sodium is the greatest determinant of the osmolality. 121  Edema Edema can be defined as palpable swelling produced by expansion of the interstitial fluid volume. Edema does not become evident until the interstitial fluid volume has been increased by 2.5 to 3 L. 122  Causes of Edema 1. Certain medical conditions such as: Heart failure, renal failure, Liver cirrhosis, Deep vein thrombosis. 2. Side effects from medication: Some drugs, like blood pressure or pain management medications, may lead to edema. 3. Poor nutrition: foods high in salt (sodium). 4. Pregnancy. 123  Regulation of Water Balance Mechanisms of Regulation: There are two main physiologic mechanisms that assist in regulating body water: thirst and antidiuretic hormone (ADH). 1. Thirst is primarily a regulator of water intake. 2. ADH a regulator of water output. Both mechanisms respond to changes in extracellular osmolality and volume. (Increase extracellular osmolality and decrease in blood volume) 124  Thirst Thirst is controlled by the thirst center in the hypothalamus. There are two stimuli for true thirst based on water need: (1) Cellular dehydration caused by an increase in extracellular osmolality. (2) Decrease in blood volume. Sensory neurons, called osmoreceptors, which are located in or near the thirst center in the hypothalamus, respond to changes in extracellular osmolality by stimulating the sensation of thirst. 125  Anti Diuretic Hormone Antidiuretic Hormone: The reabsorption of water by the kidneys is regulated by ADH, also known as vasopressin. ADH is synthesized in the hypothalamus, transported for storage in the posterior pituitary and then released into the circulation. 126 127  Diabetes insipidus (DI) Caused by a deficiency of or a decreased response to ADH. Persons with DI are unable to concentrate their urine during periods of water restriction; they excrete large volumes of urine, usually 3 to 20 L/day, depending on the degree of ADH deficiency or renal insensitivity to ADH. This large urine output is accompanied by excessive thirst. Inadequate fluid intake leads to hypertonic dehydration and increased serum osmolality. 128 The Syndrome of Inappropriate ADH (SIADH) Results from a failure of the negative feedback system that regulates the release and inhibition of ADH. In persons with this syndrome, ADH secretion continues even when serum osmolality is decreased, causing marked water retention and dilutional hyponatremia. 129 Evaluation: Patients usually present with hyponatremia. The Schwartz and Bartter Clinical Criterion 1. Serum Na less than 135mEq/L 2. Serum osmolality less than 275 mOsm/kg 3. Urine Na greater than 40 mEq/L 4. Urine osmolality greater than 100 mOsm/kg The target is always to correct hyponatremia. 130  Isotonic Fluid Volume Deficit Fluid volume deficit occurred when the loss of extracellular fluid exceeds intake of water. (loss of ECF > intake). Water and electrolytes are lost in the same proportion as they exist in normal body fluids. Causes: fluid loss from vomiting, diarrhea, GI suctioning, sweating, decreased fluids intake, exercise, fever, burn. Risk factors: Diabetes insipidus, Adrenal insufficiency, Osmotic diuresis, Hemorrhage, Coma. 131 Acid – Base Balance 132  Acid – Base Balance Normally, the concentration of body acids and bases is regulated so that the pH of extracellular body fluids is maintained within a very narrow range of 7.35 to 7.45. This balance is maintained through mechanisms that generate, buffer, and eliminate acids and bases. Regulation of pH The pH of body fluids is regulated by three major mechanisms: 1. ICF and ECF buffering systems. 2. The lungs, which control the elimination of CO2. 3. The kidneys, which eliminate H+ and regulate the elimination of HCO3. 133 134 Interpretation Guidelines 135  Step 1: pH Look at pH. pH is an indicator of H+ ion concentration. If within normal range, or outside normal limits. Assess whether acidosis or alkalosis is present. The normal range for pH is Between 7.35-7.45. The middle of the normal range of pH is 7.40. If the pH. is less than 7.35 (pH7.45), it’s called alkalosis. If the pH is less than 6.8 or more than 7.8 death occurred. 136  Step 2: PaO2 PaO2 : Partial pressure of oxygen in the arterial blood Assess hypoxemic state. The normal range for PaO2 is between 80 -100 mmHg. If PaO2 is 100 mmHg, a Hyperoxic state exists. 137  Step 3: PaCO2 PaCO2 : Patrial pressure of carbon dioxide in the arterial blood. PaCO2: Represent a respiratory component. Assess ventilatory status. The normal range for PaCO2 is between 35-45 mmHg. If PaCO2 is less than 35 (PaCO2 45 mmHg), it is called acidosis. (Ventilatory failure or hypercarbia). 138  Step 4: HCO3- HCO3-: Is Bicarbonate. HCO3-: Represent metabolic component. Assess metabolic component. The normal range for HCO3- is between 22-28 mEq/l. If bicarbonate is less than 22 (HCO3- < 22 mEq/l), it is called acidosis. If bicarbonate is more than 28 (HCO3- > 28 mEq/l), it is called alkalosis. 139 140  Hypovolemic Shock Shock: Inadequate blood flow to tissues and cells of the body. Hypovolemic shock resulting from decreased intravascular volume due to fluid loss. Manifestation: Hypotension, tachycardia, cool and pale skin, cyanosis, and decreasing urinary output. 141 The End 142 Hematology System 143 Alterations in Platelets (Thrombocytes) 144  Mechanism of Hemostasis The term hemostasis refers to the stoppage of blood flow. Hemostasis is orderly, stepwise process for stopping bleeding. Hemostasis is divided into five stages: vessel spasm, formation of the platelet plug, blood coagulation or development of an insoluble fibrin clot, clot retraction, and clot dissolution. 145  Hypercoagulability States Hypercoagulability represents hemostasis in an exaggerated form and predisposes to thrombosis. Arterial thrombi caused by turbulence blood flow and composed of platelet aggregates. Venous thrombi caused by stasis of flow are largely composed of platelet aggregates and fibrin complexes. 147 148  Thrombocytosis The term thrombocytosis is used to describe platelet counts greater than 1,000,000/mm. This occurs in some malignancies and inflammatory states and after splenectomy. 149  Thrombocytopenia Thrombocytopenia represents a decrease in the number of circulating platelets (usually less than 100,000/mm3). It can result from decreased platelet production by the bone marrow, increased pooling of platelets in the spleen, or decreased platelet survival caused by immune or nonimmune mechanisms. 150  Coagulation Defects Impairment of blood coagulation can result from deficiencies of one or more of the known clotting factors, and predisposes to bleeding. Deficiencies can occur because: 1. Defective synthesis (Liver disease, vitamin K deficiency). 2. Inherited defects (Hemophilia A, Vonwillebrand disease). 3. Increased consumption of the clotting factors (DIC). Bleeding that results from clotting factor deficiency typically occurs after injury or trauma. 151  Hemophilia A Hemophilia A caused by a deficiency in factor VIII, is an X-linked recessive disorder that primarily affects males. The most common manifestation for Hemophilia A is Bleeding. Factor VIII replacement therapy is initiated when bleeding occurs or as prophylaxis with repeated bleeding episodes. 152 Disseminated intravascular coagulation (DIC) 153  Disseminated intravascular coagulation (DIC) Disseminated intravascular coagulation is a paradox in the haemostatic sequence and is characterized by widespread intravascular coagulation and bleeding. It is not a primary disease but occurs as a complication of a wide variety of conditions. DIC begins with massive activation of the coagulation sequence as a result of unregulated generation of thrombin. Clot formation consumes all available coagulation proteins and platelets, and severe haemorrhage results. 154 155  Conditions associated with DIC Obstetric Conditions. Cancers. Infections. Shock. Trauma or surgery. Hematological conditions (Blood transfusion reaction ). 156 Alteration in Red Blood Cells (Erythrocytes) 157  The Red Blood Cell The mature red blood cell, the erythrocyte, is a non-nucleated, biconcave disk. This shape increases the surface area available for diffusion of oxygen and allows the cell to change in volume and shape without rupturing its membrane. The two major types of normal hemoglobin are adult hemoglobin (HbA) and fetal hemoglobin (HbF). HbA consists of a pair of  chains and a pair of  chains. HbF consists of a pair of  chains and a pair of  chains ( HbF had high affinity for O2). HbF is replaced within 6 months of birth with HbA. 158 HbA HbF 159  Red Blood Cell Production The rate at which hemoglobin is synthesized depends on the availability of iron for heme synthesis. A lack of iron results in relatively small amounts of hemoglobin in the red blood cells. Most of the functional iron (80%) is found in hemoglobin. Iron in the hemoglobin compartment is recycled. Erythropoiesis is the production of red blood cells. 160  Red Blood Cell Production Red blood cell production is regulated by the hormone erythropoietin, which is produced by the kidney in response to a decrease in oxygen levels (Hypoxia). Red cells develop from stem cells in the bone marrow and are released as reticulocytes into the blood, where they become mature erythrocytes. 161  Red Blood Cells The red blood cell provides the means for transporting oxygen from the lungs to the tissues. Oxygen is transported in chemical combination with hemoglobin, and as a gas dissolved in plasma. The life span of a red blood cell is approximately 120 days. Red cell destruction normally occurs in the spleen, liver, bone marrow, and lymph nodes. In the process of destruction, the iron from the hemoglobin is returned to the bone marrow for reuse in red cell production or taken to the liver or other tissues for storage. The heme portion of the hemoglobin molecule is converted to bilirubin. Bilirubin, which is insoluble in plasma, attaches to albumin and transferred to the liver to be excreted in the bile. 162  Anemia Anemia is defined as an abnormally low hemoglobin level, number of circulating red blood cells, or both, resulting in diminished oxygen- carrying capacity of the blood. Anemia usually results from: 1. Excessive loss (i.e., bleeding). 2. Destruction (i.e., hemolysis) of red blood cells. 3. Deficient red blood cell production because of a lack of nutritional elements or bone marrow failure. Anemia is not a disease, but an indication of some disease process or alteration in body function. Clinical manifestations: weakness, fatigue, pallor, syncope, dyspnea, and tachycardia. 163  Blood Loss Anemia With anemia caused by bleeding, iron and other components of the erythrocyte are lost from the body. Blood loss may be acute or chronic. 1. Acute Blood Loss: Acute blood loss is accompanied by a loss of vascular volume and carries with it a risk of hypovolemia and shock. The hypoxia that results from blood loss stimulates red cell production by the bone marrow. 2. Chronic Blood Loss: Chronic blood loss does not affect blood volume but instead leads to iron- deficiency anemia. 164  Hemolytic Anemia Hemolytic anemia is characterized by 1. Premature destruction of red cells. 2. Retention in the body of iron and the other products of hemoglobin destruction. 3. Marked increase in erythropoiesis within the bone marrow. As with other types of anemias, the person experiences easy fatigability, dyspnea, and other signs and symptoms of impaired oxygen transport. The person may also have an increase in serum bilirubin and mild jaundice. 165  Causes of Hemolytic Anemia The cause of hemolytic anemia can be intrinsic or extrinsic to the red blood cell. Intrinsic causes include defects of the red cell membrane, the various hemoglobinopathies, and inherited enzyme defects. Acquired forms of hemolytic anemia are caused by agents extrinsic to the red blood cell, such as drugs, bacterial and other toxins, antibodies, and physical trauma. 166  Thalassemias The thalassemias result from absent or defective synthesis of the  or the  chains of hemoglobin. The -thalassemias represent a defect in  chain synthesis, and the  thalassemias represent a defect in  chain synthesis. The defect is inherited as a mendelian trait, and a person may be heterozygous for the trait and have a mild form of the disease or be homozygous and have the severe form of the disease. Two factors contribute to the anemia that occurs in the thalassemias: reduced hemoglobin synthesis and an imbalance in globin chain production. 167  Types of Thalassemia The presence of one normal gene in heterozygous persons (thalassemia minor) usually results in sufficient normal hemoglobin synthesis to prevent severe anemia. Persons who are homozygous for the trait (thalassemia major) have severe, transfusion-dependent anemia evident at 6 to 9 months of age. Severe growth retardation affects children with the disorder. Increased hematopoiesis in response to erythropoietin causes bone marrow expansion, impairs bone growth, and causes bone abnormalities. The facial and cranial bones, in particular, tend to be enlarged and distorted. 168  Aplastic Anemia Aplastic anemia (i.e., bone marrow depression) describes a primary condition of bone marrow stem cells that results in a reduction of all three hematopoietic cell lines—red blood cells, white blood cells, and platelets—with fatty replacement of bone marrow. Among the causes of aplastic anemia are exposure to high doses of radiation, chemicals, and toxins that suppress hematopoiesis directly, or through immune mechanisms. Chemotherapy and irradiation commonly result in bone marrow depression. 169  Iron-Deficiency Anemia The anemia results from dietary deficiency, loss of iron through bleeding, or increased demands. Because iron is a component of heme, a deficiency leads to decreased hemoglobin synthesis and consequent impairment of oxygen delivery. The usual reason for iron deficiency in adults is chronic blood loss because iron cannot be recycled to the pool. In men and postmenopausal women, blood loss may occur from gastrointestinal bleeding because of peptic ulcer, intestinal polyps, haemorrhoids, or cancer. Excessive aspirin intake may cause undetected gastrointestinal bleeding. 170  Iron-Deficiency Anemia Iron deficiency anemia is characterized by low hemoglobin and haematocrit values, decreased iron stores, and low serum iron and ferritin levels. The red cells are decreased in number and are microcytic and hypochromic. Poikilocytosis (irregular shape) and anisocytosis (irregular size) are also present. 171  Manifestations of iron-deficiency anemia Depending on the severity of the anemia, fatigability, palpitations, dyspnea, angina, and tachycardia may occur. Epithelial tissue atrophy is common and results in waxy pallor, brittle hair and nails, smooth tongue, sores in the corners of the mouth. 172  Megaloblastic Anemias Megaloblastic anemias are caused by abnormal nucleic acid synthesis that results in enlarged red cells (MCV >100 fL) and deficient nuclear maturation. Cobalamin (vitamin B12) and folic acid deficiencies are the most common cause of megaloblastic anemias. 1. Cobalamin (Vitamin B12) Deficiency Anemia (Pernicious anemia) Vitamin B12 serves as a cofactor for two important reactions in humans. It is essential for the synthesis of DNA. When it is deficient, nuclear maturation and cell division, especially of the rapidly proliferating red cells, fail to occur. 173  Cobalamin (Vitamin B12) Deficiency Anemia (Pernicious anemia) Other causes of vitamin B12 deficiency anemia include gastrectomy, ileal resection, and malabsorption syndromes in which vitamin B12, and other vitamin B compounds are poorly absorbed. The hallmark of vitamin B12 deficiency is megaloblastic anemia. When vitamin B12 is deficient, the red cells that are produced are abnormally large because of excess ribonucleic acid production of hemoglobin and structural protein. Neurologic symptoms that accompany this disorder are memory changes, numbness, and unsteady gait. 174  Folic Acid-Deficiency Anemia 2. Folic Acid-Deficiency Anemia Folic acid is readily absorbed from the intestine. It is found in vegetables (particularly the green leafy types), fruits, cereals, and meats. However, much of the vitamin is lost in cooking. The most common causes of folic acid deficiency are malnutrition or dietary lack. Neoplastic disease. Some drugs to treat seizure disorders. Because pregnancy increases the need for folic acid 5- to 10-fold, a deficiency commonly occurs. 175 Alterations in White Blood Cells 176  White Blood Cells (Leukocytes) The white blood cells and lymphoid tissues where these cells originate and mature function to protect the body against invasion by foreign agents. Disorders of the white blood cells includes: 1. Deficiency of leukocytes (Leukopenia). 2. Increased number of leukocytes (Leukocytosis). 177 178  NON-NEOPLASTIC DISORDERS OF WHITE BLOOD CELLS The number of leukocytes, or white blood cells, in the peripheral circulation normally ranges from 5000 to 10,000/L of blood. The term leukopenia describes an absolute decrease in white blood cell numbers. Leukopenia affect any of the specific types of white blood cells, but most often it affects the neutrophils, which are the predominant type of granulocyte. 179  Neutropenia and Agranulocytosis Neutropenia refers specifically to a decrease in neutrophils. It commonly is defined as a circulating neutrophil count of less than 1500 cells/  L. Agranulocytosis, which denotes a severe neutropenia, is characterized by a circulating neutrophil count of less than 200 cells/  L. 180  Clinical Course of the Neutropenia Because the neutrophil is essential to the cellular phase of inflammation, infections are common in persons with neutropenia. The signs and symptoms of neutropenia initially are those of bacterial or fungal infections. They include malaise, chills, and fever, followed by extreme weakness and fatigue. The most frequent site of serious infection is the respiratory tract, a result of bacteria, fungi, and protozoa that frequently colonize the airways. Ulcerative necrotizing lesions of the mouth are common in neutropenia. Ulcerations of the skin, vagina, and gastrointestinal tract also may occur. 181 NEOPLASTIC DISORDERS OF HEMATOPOIETIC AND LYMPHOID ORIGIN The leukemias are malignant neoplasms of cells originally derived from hematopoietic stem cells. (Cancer of Leukocytes). They are characterized by diffuse replacement of bone marrow with unregulated, proliferating, immature neoplastic cells. They have a long-life span, don’t function normally, circulate in the blood stream, interfere with the maturation of normal blood cells, and infiltrate many body organs. The causes of leukemia are unknown. The incidence of leukemia among persons who have been exposed to high levels of radiation is unusually high. 182  Lymphoma The lymphomas represent solid tumours derived from neoplastic lymphoid tissue cells (i.e., lymphocytes). Cancers affect lymphatic system, and lymphatic cells. Tow types: Hodgkin’s lymphoma and non-Hodgkin’s lymphoma. 183  Hodgkin’s Lymphoma Hodgkin’s disease is a specialized form of lymphoma that features the presence of an abnormal cell called a Reed-Sternberg cell. Reed-Sternberg cells begins as a malignancy in a single lymph node and then spreads to contiguous lymph nodes. The cause of Hodgkin’s disease is unknown. Although exposure to carcinogens or viruses as well as genetic and immune mechanisms have been proposed as causes. Hodgkin’s disease is characterized by painless and progressive enlargement of a single node or group of nodes. 184  Non-Hodgkin’s Lymphomas Non-Hodgkin's lymphomas represent a group of heterogeneous lymphocytic cancers that are multicentric in origin and spread to various tissues throughout the body, including the bone marrow. The cause of most of the non-Hodgkin’s lymphomas is unknown. A viral cause is suspected in at least some of the lymphomas. 185 The End 186 187  Introduction Homeothermic: Humans capable of maintaining their body temperatures within narrow limits. 410 C - 430 C convulsions are seen Nerve malfunction & protein denaturation seen with higher temperature. 188  Measured under tongue, axilla or rectum. Oral temp is 0.50C less than core body temperature (rectal temp). Internal temp varies with activity pattern and changes in external temp. Circadian fluctuation of about 10C - lowest at night and highest during the day. Women show higher temp during second half of the menses. 189  Definitions It is the somatic sensation of heat or cold. It is the degree of or intensity of heat of a body in relation to external environment. The body temperature is the difference between the amount of heat produced by body processes & the amount of heat lost to the external environment. 190 Temperature Regulation Body Temperature =Thermogenesis – Heat Loss 191  Types of Temperature Measurement 1. Core temperature: it is the temperature of internal body tissues below the skin & subcutaneous tissues. The sites of measurement are rectum, tympanic membrane, esophagus, pulmonary artery & urinary bladder. 192 2. Surface body temperature: it refers to the body temperature of external body tissues at the surface that is of the skin & subcutaneous tissues. The sites of measurement are orally and axillary. 193  Physiology of thermoregulation It is precisely regulated by physiological & behavioral mechanisms in number of ways:- 1. Neural control. 2. Vascular control. 3. Skin in temperature regulation. 4. Behavioral control. 194 Factors Affecting Body Temperature AGE EXERCISE HORMONAL LEVEL STRESS CIRCARDIAN RHYTHM ENVIRONMENT 195 196 197  Fever Fever is an elevation of body temperature that exceeds normally daily variation and occurs in conjunction with an increase in the hypothalamic set point for e.g. 37⁰C - 39⁰C. 198  Classification Or Patterns Of Fever 1. Intermittent fever: Temperature returns to acceptable value at least once in 24 hours. The temperature curve returns to normal during the day and reaches its peak in the evening. E.g.- in septicemia. 2. Remittent fever: Fever spikes & falls without a return to the normal temperature levels. The temperature fluctuates but does not return to normal. E.g.- TB, viral diseases, bacterial infections 199 3.Sustained fever: The temperature remains continuously elevated above 38 degree Celsius & demonstrates little fluctuation. 4. Relapsing fever: Periods of febrile periods interspersed with acceptable temperature values i.e., periods of fever are interspersed with periods of normal temperature. 200  Hyperthermia It is elevated body temperature due to failed thermoregulation that occurs when a body produces or absorbs more heat than it dissipates. Temperature ranges > 37.5 - 38.3 degree Celsius. 201  Causes of Hyperthermia 1. Heat Stroke: Prolonged exposure to sun or high environmental temperatures. A dangerous heat emergency with a high mortality rate. 202 203  Hypothermia Hypothermia is a state in which the core body temperature is lower than 35 degree Celsius. At this temperature many of the compensatory mechanism to conserve heat begin to fall. 204  Risk Factors For Hypothermia Age extremes: elderly, neonates. Outdoor exposure: occupational, sports related, inadequate clothing. Immobility. Drugs and intoxicants. Malnutrition 205  Signs and Symptoms Lethargy Shivering Lack of Coordination Pale, cold, dry skin Early rise in heart rate, and respiratory rates. In severe Hypothermia Low blood pressure, Undetectable pulse and respirations, and Cardiac arrest. 206 The End 207 Stress and Adaptation 208  Definitions Homeostasis: A state of balance in the body or equilibrium among the physiologic, psychological, socio-cultural, intellectual, and spiritual needs of the body. Stress: A disruptive condition that occurs in response to any demand made on the body, such demands are called stressors. Two types of stress: 1. Eustress is stress that presents the opportunity for growth and satisfaction. 1. Distress is negative stress that can result in debilitative strain. 209  Definitions Stressor: Any physical, social, or psychological event or condition that causes a disruption in homeostasis and causes the stress response. Stress response: A state of physiological and behavioral responses to a stressor that help to restore homeostasis. Adaptation: Restoration of homeostasis (the adjusting behavior to certain situations that enable the person to cope with these situations). Coping: Is the cognitive and behavioral strategies used to manage the stressor 210  Common stressors Physiological: Aging, injury, infection, pain, noise, pollution. Psychological: Fear, insecurity, failing in task, loss of family member. Social: Isolation, poverty, threat to safety. Spiritual: Guilt, doubt, hopelessness. 211  Factors affecting an individual response to stress 1. Internal: Age Gender Health status Nutritional status Previous experiences 2. External: Social support Cultural Religious Number, time and duration of stressors. 212  Psychological response to stress 1. Individual’s perception of the event: The way you interpreted the event is how you respond to the event. Appraisal of the stressful event A. Primary appraisal: Identification, assessment of the situation. B. Secondary appraisal: Evaluation and action. 2. Coping with the stressful event A. Cognitive (develop emotions) or B. Behavioral efforts (changes in the environment) 213  Physiological responses to stress 1. Local adaptation syndrome. 2. General adaptation syndrome. 1. Local adaptation syndrome: Responses that occur at the local site of injury such as redness and swelling. 214  Physiological responses to stress 2. General adaptation syndrome (GAS): Has three stages:- Stage 1: Alarm: The body initially responds to a stressor with changes that lower resistance. Crisis/alarm (paleness, shivering, sweating of palms) Sympathetic stimulation Stage 2: Resistance: If the stressor continues, the body mobilizes to withstand the stress and return to normal. Adaptation. Begins almost immediately after beginning of alarm phase. Body adjusts in order to return to homeostasis. Parasympathetic nervous system helps keep energy levels under control. 215  Physiological responses to stress Stage 3: Exhaustion: Ongoing, extreme stressors eventually deplete the body’s resources, so we function at less than normal. If adaptive energy is inadequate to deal with prolonged or overwhelming stress. Occurs after continuous alarm and resistance reactions. Physical and emotional energy to battle stress have been depleted. 216  General adaptation syndrome Resistance: If the stressor continues, the body mobilizes to with Exhaustion: stand the stress and Ongoing, extreme return to normal. stressors eventually deplete the body’s Alarm: resources so we The body initially function at less responds to a than normal. stressor with changes that lower resistance. Homeostasis: The body systems maintain a stable and consistent (balanced) state. Stressor: The stressor Return to may be homeostasis threatening or Illness and Death: exhilarating. Illness In extreme or chronic cases, exhaustion can become so pronounced that death can occur. Death 217  Effects of Stress on the Body Hypertension, Tachycardia, Tachypnea. Eczema and psoriasis. Muscular twitches. Weight gain. Headaches, and Disrupted sleep. Mouth ulcers. Complications: Stroke and heart attack, Renal Hypertension, Depression, immune system suppression. 218  Coping strategies Healthy Unhealthy Relaxation Smoking Meditation Drugs Pets Alcohol Exercise Overeating Massage Music Religious Books Communication 219 The End 220 Burns  The Skin The skin is the body’s largest organ and the primary defense against pathogenic invasion. The skin contributes to temperature regulation, prevents loss of internal fluids, and provides sensory awareness. The Skin is consisting of three layers: 1. Epidermis: Outer Layer. 2. Dermis: Middle Layer. 3. Hypodermis (Subcutaneous tissue): Inner Layer.  Burn Burn is an injury to the skin or other organic tissue primarily caused by heat or due to radiation, electricity, or contact with chemicals. Burns are caused by a transfer of energy form a heat source to the body, causing tissue destruction.  Burn Factors determine the severity of burn injury: Age: morbidity and mortality increased with children & elderly. Depth of the burn. Body surface area that is burned. Presence of inhalation injury. Presence of other injuries. Classification of Burns according to Depth 1. First Degree Burn (Superficial) Caused by sunburn Involve Epidermis. Manifestations: Pain, tingling, itching, peeling. 2. Second Degree Burn (Partial thickness) Caused by flash flame. Involve epidermis and portion of dermis. Manifestations: Pain, Hyperesthesia, sensitive to cold air.  Classification of Burns according to Depth 3. Third Degree (full thickness) Caused by flame, hot liquids, electric & chemical. Involve epidermis, dermis, subcutaneous connective tissues, and muscle may involved. Manifestations: Pain free, Shock, Hematuria.  Zones of Burn Injury Zone of coagulation: the innermost area, where cellular death occurs, the most damage. Zone of stasis: the middle area has a compromised blood supply, inflammation and tissue injury. Zone of hyperemia: the outermost area sustains the least damage.  Methods to estimate the total body service area (TBSA) affected by burns 1. Rule of Nines The system divides the body into multiples of nine. The sum of these parts equals the total body surface area. 2. Palm method Used in patients with scattered burns. The size of the patient hand including fingers is approximately 1% of the patient TBSA. 22  Effects of Burn Injury 1. Fluid loss 2. Infection 3. Hypothermia 4. Scarring 5. Compromised immunity 6. Changes in function, appearance, and body image. Burns 20% TBSA produce systemic response (hemodynamic instability)  Effects of Burn Injury 1. Cardiovascular effects Hypovolemia Cardiac output decreases, and Blood pressure decreased. Heart rate increased 2. Edema & Electrolyte Edema increases and may lead to compartment syndrome. Hyponatremia Hyperkalemia Hypokalemia  Effects of Burn Injury 3. Upper airway injury 4. Lower airway injury Tissue hypoxia Bronchospasm Atelectasis 5. Renal alterations Renal Failure Acute Tubular Necrosis  Effects of Burn Injury 6. Immunologic alterations High risk for infection and sepsis 7. Thermoregulation alterations Inability to regulate body temperature. 8. Gastrointestinal Alterations Paralytic ileus Acute gastric erosion Vomiting Gastric bleeding The End